SHOCKBY DR KAUSAR MALIKAssistant professor Medicine

Shock occurs when the rate of arterial blood flow is inadequate to meet tissue metabolic needs.

SHOCK

Regional hypoxia

Subsequent lactic acidosis from anaerobic metabolism

in peripheral tissues End-organ damage and failure.

Classification

Hypovolemic shockCardiogenic shockObstructive shock Distributive shock

Hypovolemic shock

Loss of blood (hemorrhagic shock) External hemorrhage

Trauma Gastrointestinal tract bleeding

Internal hemorrhage Hematoma Hemothorax or hemoperitoneum

Loss of plasma Burns

Hypovolemic shock Loss of fluid and electrolytes

External Vomiting Diarrhea Excessive sweating Hyperosmolar states (diabetic ketoacidosis, hyperosmolar nonketotic

coma) Internal ("third spacing")

Pancreatitis Ascites Bowel obstruction

Cardiogenic shock

Dysrhythmia Tachyarrhythmia Bradyarrhythmia

"Pump failure" (secondary to myocardial infarction or other cardiomyopathy)

Acute valvular dysfunction (especially regurgitant lesions) Rupture of ventricular septum or free ventricular wall

Obstructive shock Tension pneumothorax Pericardial disease (tamponade, constriction) Disease of pulmonary vasculature (massive pulmonary

emboli, pulmonary hypertension) Cardiac tumor (atrial myxoma) Left atrial mural thrombus Obstructive valvular disease (aortic or mitral stenosis)

Distributive shock Septic shock Anaphylactic shock Neurogenic shock Vasodilator drugs Acute adrenal insufficiency

Clinical FindingsHypotension

A systolic blood pressure of 90 mm hg or less or A mean arterial pressure of < 60–65 mm hg Must be evaluated relative to the patient's

normal blood pressure.

Hypotension

POSTURAL DROP A drop in systolic pressure of more than 10–20

mm Hg an increase in pulse of more than 15 beats per

minute with positional change suggests depleted intravascular volume.

Hypotension

However, blood pressure is often not the best indicator of organ perfusion because compensatory mechanisms, such as increased heart rate, contractility, and vasoconstriction can occur to prevent hypotension.

Clinical FindingsCool or mottled extremities Weak or thready peripheral pulses. Splanchnic vasoconstriction

oliguria, bowel ischemia, and hepatic dysfunction

Clinical FindingsPatients may become restless, agitated, confused,

lethargic, or comatose as a result of inadequate perfusion of the brain. .

Hypovolemic shock Oliguria, altered mental status, and cool

extremitiesJugular venous pressure is low, and There is a narrow pulse pressure indicative of

reduced stroke volume. Rapid replacement of fluids restores tissue

perfusion

cardiogenic shockSigns of global hypoperfusion with oliguriaAltered mental status, andCool extremities.Jugular venous pressure is elevated. There may be evidence of pulmonary edema in the

setting of left-sided heart failure.

obstructive shock In, the central venous pressure may be elevated but the TEE

or TTE may show reduced left ventricular filling, a layer of fluid between the pericardium as in the case of tamponade, or thickened pericardium as in the case of pericarditis.

Pericardiocentesis or pericardial window –cardiac temponade Chest tube placement-pneumothorax

Catheter-directed thrombolytic therapy-pulmonary embolism

Distributive shockhyperdynamic heart sounds, warm extremities initially, and a wide pulse pressure indicative of large stroke

volume. The echocardiogram may show hyperdynamic left

ventricle. Fluid resuscitation may have little effect on blood

pressure, urinary output, or mentation.

Septic shock clinical evidence of infection in the setting of

persistent hypotension and evidence of organ hypoperfusion, such as lactic acidosis, decreased urinary output, or altered mental status despite volume resuscitation.

Neurogenic shockCentral nervous system injury and Persistent hypotension despite volume

resuscitation.

APPROACH TO THE PATIENT

Obtain history for underlying cause, including • Known cardiac disease (coronary disease, CHF,

pericarditis) • Recent fever or infection (leading to sepsis) • Drugs, e.G., Excess diuretics or antihypertensives • Conditions predisposing for pulmonary embolism • possible bleeding from any site, particularly GI

tract.

PHYSICAL EXAMINATION Jugular veins are flat in oligemic or distributive

shockJugular venous distention(JVD) suggests

cardiogenic shock JVD in presence of paradoxical pulse may reflect

cardiac tamponade

PHYSICAL EXAMINATION

Evidence of CHF Murmurs of aortic stenosis, Acute regurgitation (mitral or aortic), ventricular

septal defect.Check for asymmetry of pulses (aortic dissection) Tenderness or rebound in abdomen may indicate

peritonitis or pancreatitis;High-pitched bowel sounds suggest intestinal

obstruction.

LABORATORY

Obtain hematocrit, WBC, electrolytes. If actively bleeding, check platelet count, PT, PTT, DIC

screen. Arterial blood gas usually shows metabolic acidosis

If sepsis suspected, drawblood cultures, perform urinalysis, and obtain Gram stain and cultures of sputum, urine, and other suspected sites.

Obtain ECG (myocardial ischemia or acute arrhythmia), chest x-ray (CHF ,tension pneumothorax, aortic dissection,

pneumonia). Echocardiogram maybe helpful (cardiac tamponade, CHF).

Central venous pressure or pulmonary capillary wedge (PCW) pressure measurements may be necessary to distinguish between different categories of shock

Mean PCW < 6 mmHg suggests oligemic or distributive shock

PCW > 20 mmHg suggests left ventricular failure.

TREATMENTAimed at rapid improvement of tissue

hypoperfusion and respiratory impairmentSerial measurements of BP (intraarterial line

preferred), heart rate, continuous ECG monitor, urine output, pulse oximetry

Blood studies: HCT, electrolytes ,creatinine, BUN, ABGS, ph,

calcium, phosphate, lactate, urine Na concentration (<20 mmol/L suggests volume depletion)

Consider continuous monitoring of CVP and/or pulmonary artery pressure, with serial PCW pressures in pts with ongoing blood loss or suspected cardiac dysfunction.

• Insert Foley catheter to monitor urine flow. • Assess mental status frequently

Augment systolic BP to >100 mmHg: (1) place in reverse trendelenburg position; (2) IV volume infusion (500- to 1000-ml bolus),

unless cardiogenic shock suspectedBegin with normal saline, then whole blood,or

packed RBCS, if anemic Continue volume replacement as needed to

restore vascular volume

Medications

Vasoactive TherapyVasopressors and inotropic agents are

administered only after adequate fluid resuscitation.

Choice of vasoactive therapy etiology of shock cardiac output.

If there is evidence of low cardiac output with high filling pressures, inotropic support is needed to improve contractility.

If there is continued hypotension with evidence of high cardiac output after adequate volume resuscitation, then vasopressor support is needed to improve vasomotor tone.

Dobutamine Adrenergic agonist, First-line drug for cardiogenic shock, increasing contractility and

decreasing afterload. The initial dose is 0.5–1 mcg/kg/min as a continuous intravenous

infusion, which can be titrated every few minutes as needed to hemodynamic effect;

The usual dosage range is 2–20 mcg/kg/min intravenously.

Norepinephrine Alpha -adrenergic and beta -adrenergic agonist, It preferentially increases mean arterial pressure over cardiac

output. .

Epinephrine, Both alpha-adrenergic and beta -adrenergic effects, May be used in severe shock and during acute resuscitation. It is the vasopressor of choice for anaphylactic shock

Dopamine variable effects according to dosage. At low doses (2–5 mcg/kg/min intravenously), stimulation of

dopaminergic and -adrenergic receptors produces increased glomerular filtration, heart rate, and contractility.

At doses of 5–10 mcg/kg/min, 1-adrenergic effects predominate, resulting in an increase in heart rate and cardiac contractility.

At higher doses (> 10 mcg/kg/min), -adrenergic effects predominate, resulting in peripheral vasoconstriction.

Vasopressin (antidiuretic hormone or ADH) is often used as an adjunctive therapy to catecholamine vasopressors in the treatment of distributive or vasodilatory shock.

Antibiotics

Definitive therapy for septic shock includes an early initiation of empiric broad-spectrum antibiotics after appropriate cultures have been obtained.

Imaging studies may prove useful to attempt localization of sources of infection.

Surgical management may also be necessary if necrotic tissue or loculated infections are present (see Table 30–9).